RASAL1 in Thyroid Cancer: Wisdom From an Old Foe
Menée sur 101 échantillons tumoraux prélevés sur des patients atteints d'un cancer de la thyroïde, puis in vitro et in vivo, cette étude met en évidence le rôle de suppresseur de tumeurs joué par le gène RASAL1
True therapeutic success in oncology relies on a sound understanding of the molecular arena of the cancer in question. Thyroid cancer has rapidly increased in global incidence in recent decades (1). Papillary thyroid cancer (PTC) and follicular thyroid cancer (FTC) are differentiated thyroid cancers (DTCs), which account for more than 90% of all thyroid malignancies. Most DTCs are indolent tumors and are usually curable. However, in surgically inoperable, radioiodine-refractory DTCs and in poorly differentiated tyroid cancers and anaplastic thyroid cancers (ATCs), the prognosis is poor with no effective treatment available. Although much progress has been made in understanding the molecular mechanisms of thyroid cancer in the past 5 to 10 years, as demonstrated by the elucidation of the role the MAPK and PI3K–AKT pathways play in differentiated thyroid cancer (2). Mutations in these two key signaling pathways, in genes such as RAS, BRAF, PI3KCA, and PTEN, account for 65% to 70% of DTCs (2). In this issue of the Journal, Liu and colleagues add to our current understanding of thyroid tumorigenesis by providing a compelling study of how alternative RAS signaling–related genes impact on thyroid tumorigenesis (3). Compared with normal human thyroid tissue, the RAS GTPase-activating protein (RasGAP) gene, RASAL1, was commonly silenced in the thyroid cell lines surveyed, with consistently low mRNA and protein …